Effects of total glucosides of peony on expression of inflammatory cytokines and phosphorylated MAPK signal molecules in hippocampus induced by fibrillar Aβ42.
- Author:
Dehong HUANG
1
;
Mengyuan LIU
;
Xiaofeng YAN
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; drug therapy; Amyloid beta-Peptides; metabolism; toxicity; Animals; Cytokines; analysis; Female; Glucosides; pharmacology; therapeutic use; Hippocampus; metabolism; JNK Mitogen-Activated Protein Kinases; metabolism; MAP Kinase Signaling System; drug effects; Mitogen-Activated Protein Kinases; metabolism; Paeonia; chemistry; Peptide Fragments; metabolism; toxicity; Phosphorylation; Rats; Rats, Sprague-Dawley; p38 Mitogen-Activated Protein Kinases; metabolism
- From: China Journal of Chinese Materia Medica 2011;36(6):795-800
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effects of hippocampal Abeta42 deposition on the expression of inflammatory cytokines and phosphorylated MAPK signal molecules as well as the intervention of AD by total glucosides of paeony (TGP).
METHOD12 week-old female SD rats were stereotactic injected one-time with a fibrillar Abeta42 positioning hippocampus to replicate AD pathology model and interfered with TGP. The expression of inflammatory cytokines and phosphorylated MAPK pathway signaling molecules were observed by immunohistochemistry (SABC), and SABC images were analyzed by image analysis software.
RESULTCompared with the control group, the IL-1beta, IL-6 and p-p38, p-JNK, p-MEK3/6 positive stained areas of AD pathology model group increased and their staining intensity decreased (the protein expression quantity inversely proportional to the staining intensity), while the IL-1beta, IL-6 and p-p38, p-JNK, p-MEK3/6 positive stained areas of the treatment groups decreased and their staining intensity increased compared with AD pathology model group.
CONCLUSIONAbeta42 deposition in hippocampus can induce the brain inflammation and the over-expression of IL-1beta, IL-6 and p-p38, p-JNK, p-MEK3/6. Inhibiting the over-expression of inflammatory cytokines and phosphorylated MAPK signaling molecules may be a major antagonistic mechanism of TGP against AD.
